Abstract
Afterload reduction in chronic asymptomatic aortic regurgitation might retard left ventricular enlargement and hypertrophy and, consequently, delay the onset of myocardial dysfunction and the need for surgical intervention. Since afterload is best expressed as wall stress, the effect of nitroglycerin on wall stress was determined in 10 normal subjects and in eight asymptomatic subjects with aortic regurgitation and normal left ventricular and circulatory function. Peak and end-systolic wall stress were estimated using a noninvasive echocardiographic technique. At rest, despite significantly larger left ventricular dimensions in the subjects with aortic regurgitation, peak systolic wall stress in this group (134 ± 29 × 10 3 dynes/cm 2) was similar to that in normal subects (134 ± 26 × 10 3 dynes/cm 2). In contrast, end-systolic wall stress was higher in aortic regurgitation (84 ± 12 versus 59 ± 15 × 10 3 dynes/cm 2) (P < 0.01). Following the administration of nitroglycerin, the subjects with aortic regurgitation had larger reductions in left ventricular end-diastolic (3.5 mm) and end-systolic (3.1 mm) dimensions than did the normal subjects (0.6 and 1.1 mm, respectively), despite similar changes in blood pressure. This resulted in normalization of end-systolic wall stress and in reduction of peak systolic wall stress below normal in aortic regurgitation. We conclude that (1) nitroglycerin offers a simple and effective means of acutely reducing afterload in asymptomatic aortic regurgitation; (2) left ventricular dimensional changes after the administration of nitroglycerin are larger in subjects with aortic regurgitation than in normal subjects. Consequently, unloading therapy may be effective in protecting the left ventricle in this disorder.
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